CCRL2 as a Radioligand Therapy Target
CCRL2, C-C motif chemokine receptor like 2, is a cell-surface protein (membrane receptor). In Human Protein Atlas immunohistochemistry, CCRL2 staining is highest in liver cancer (100% of samples positive), thyroid cancer (100% of samples positive) and lung cancer (91% of samples positive). Published literature reports that CCRL2 internalizes after ligand binding, which helps retain a radionuclide inside tumor cells. Clinical status: Discovery-stage (no clinical drug program).
Is CCRL2 a good radioligand therapy target?
Scored against the six criteria that decide whether a protein can become a radioligand therapy:
- ✅ Cell-surface accessibility: Localized to the cell surface, so a radioligand can reach it from circulation.
- ✅ Tumor expression: High IHC staining in liver cancer, 100% of samples positive.
- ✅ Internalization: Reported to internalize, which favors radionuclide retention.
- ⚠️ Clinical precedent: Discovery-stage (no clinical drug program)
- ❔ Shedding: Not yet assessed.
- ❔ Normal-tissue dosimetry: Check kidney, liver, bone marrow and salivary expression in the Human Protein Atlas tissue atlas.
CCRL2 expression in cancer
Protein expression of CCRL2 across 20 cancer types from Human Protein Atlas immunohistochemistry. The score is a weighted staining intensity from 0 to 1; "% positive" is the share of patient samples with detectable staining.
| Cancer type | IHC score | Level | % positive |
|---|---|---|---|
| Liver Cancer | 0.75 | High | 100% |
| Thyroid Cancer | 0.67 | High | 100% |
| Lung Cancer | 0.64 | High | 91% |
| Pancreatic Cancer | 0.58 | High | 82% |
| Kidney Cancer | 0.56 | High | 92% |
| Colorectal Cancer | 0.53 | High | 83% |
| Ovarian Cancer | 0.53 | High | 75% |
| Breast Cancer | 0.52 | High | 82% |
| Neuroendocrine Tumors | 0.50 | Medium | 100% |
| Melanoma | 0.44 | Medium | 78% |
| Lymphoma | 0.39 | Medium | 64% |
| Prostate Cancer | 0.39 | Medium | 75% |
| Cervical Cancer | 0.39 | Medium | 67% |
| Gastric Cancer | 0.39 | Medium | 67% |
| Endometrial Cancer | 0.36 | Medium | 58% |
| Head and Neck Cancer | 0.25 | Medium | 50% |
| Bladder Cancer | 0.18 | Low | 46% |
| Skin Cancer | 0.12 | Low | 36% |
| Glioma | 0.07 | Low | 22% |
| Testicular Cancer | 0.06 | Low | 8% |
Is CCRL2 internalized?
Yes. Cell membrane analysis of CCRL2-transfected cells revealed a weak, constitutive, ligand-independent internalization, and recycling of CCRL2.
Sources: PMID 35040613 · PMID 29056935 · PMID 28603493 · PMID 27716822 · PMID 20002784. AI-extracted from abstracts, so verify before citing.
CCRL2 clinical trials
Discovery-stage (no clinical drug program). Nuclens hasn't indexed trials for CCRL2 yet. Search ClinicalTrials.gov for CCRL2 trials.
CCRL2 normal tissue expression
Normal-tissue expression in dose-limiting organs (kidney, liver, bone marrow, salivary glands) drives radioligand dosimetry risk. Nuclens is re-validating its normal-tissue values, so they are not shown here yet. See CCRL2 in the Human Protein Atlas tissue atlas, and read how normal-tissue expression predicts radioligand dosimetry risk.
CCRL2 gene essentiality (DepMap)
CRISPR knockout effect across 1245 cancer cell lines: -0.00 (not essential). Radioligands kill by radiation, not by blocking the target, so essentiality matters less than for inhibitors. A non-essential target can still be an excellent radioligand target.
Related liver cancer radioligand targets
EGFR · c-MET (MET) · HER3 (ERBB3) · SSTR2 · STEAP2 · HER2 (ERBB2) · Mesothelin (MSLN) · B7-H3 (CD276)
See all radioligand therapy targets in liver cancer.
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Subcellular localization: UniProt via Open Targets (CC BY 4.0 / CC0). Tumor immunohistochemistry: Human Protein Atlas (CC BY-SA 4.0). Clinical trials: ClinicalTrials.gov (public domain). Gene essentiality: DepMap (CC BY 4.0). Internalization and shedding: AI-extracted from PubMed abstracts, so verify against the cited papers before relying on them. Nuclens is a first-pass triage layer, not a substitute for wet-lab validation or clinical dosimetry. Derived expression data on this page is shared under CC BY-SA 4.0.